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We began analyzing https://link.springer.com/article/10.1007/s00424-003-1012-4, but it redirected us to https://link.springer.com/article/10.1007/s00424-003-1012-4. The analysis below is for the second page.

Title[redir]:
BK channel openers inhibit migration of human glioma cells | Pflügers Archiv - European Journal of Physiology
Description:
Large-conductance Ca2+-activated K+ channels (BK channels) are highly expressed in human glioma cells. However, less is known about their biological function in these cells. We used the patch-clamp technique to investigate activation properties of BK channels and time-lapse microscopy to evaluate the role of BK channel activation in migration of 1321N1 human glioma cells. In whole cells, internal perfusion with a solution containing 500 nM free Ca2+ and external application of the BK channel opener phloretin (100 µM) shifted the activation threshold of BK channel currents toward more negative voltages of about −30 mV, which is close to the resting potential of the cells. The concentration of intracellular Ca2+ in fura-2-loaded 1321N1 cells was measured to be 235±19 nM and was increased to 472±25 nM after treatment with phloretin. Phloretin and another BK channel opener NS1619 (100 µM) reduced the migration velocity by about 50%. A similar reduction was observed following muscarinic stimulation of glioma cells with acetylcholine (100 µM). The effects of phloretin, NS1619 and acetylcholine on cell migration were completely abolished by co-application of the specific BK channel blockers paxilline (5 µM) and iberiotoxin (100 nM). The phloretin-induced increase in intracellular Ca2+ was unaffected by the removal of extracellular Ca2+ and co-application of paxilline. These findings indicate that glioma cell migration was inhibited through BK channel activation, independent of intracellular Ca2+.

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Custom-built

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Keywords {🔍}

cells, google, scholar, pubmed, cas, channels, article, channel, migration, human, glioma, kraft, cell, patt, activation, access, ion, intracellular, potassium, privacy, cookies, content, basrai, astrocytoma, pharmacol, jena, publish, search, inhibit, robert, phloretin, currents, open, calcium, schwab, physiol, institut, berlin, germany, function, data, information, log, journal, research, krause, liebmann, opener, muscarinic, blockers,

Topics {✒️}

large conductance ca2+-activated neuroligand-triggered calcium signalling month download article/chapter smooth muscle cells potassium channel blockers fura-2-loaded 1321n1 cells ion channels friedrich-schiller-universität jena human glioblastoma cells bk channel currents bk channel activation full article pdf + channel-dependent migration human astrocytoma cells privacy choices/manage cookies transformed glial cells potassium currents related subjects voltage-gated human glioma cells glioma cell migration rat glioma cells forschung und kunst human meningioma cells human melanoma cells bk channels article kraft müller glial cells intracellular ca2+ release investigate activation properties european economic area patch-clamp technique time-lapse microscopy phloretin-induced increase post-munson dj starrett je jr smith iii ab mycotoxin paxilline inhibits porcine coronary artery check access instant access cerebellar granule cells conditions privacy policy intracellular ca2+ distribution lum-ragan jt freie universität berlin accepting optional cookies astrocytoma cells grants tmwfk b301–96085 500 nm free ca2+

Schema {🗺️}

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         description:Large-conductance Ca2+-activated K+ channels (BK channels) are highly expressed in human glioma cells. However, less is known about their biological function in these cells. We used the patch-clamp technique to investigate activation properties of BK channels and time-lapse microscopy to evaluate the role of BK channel activation in migration of 1321N1 human glioma cells. In whole cells, internal perfusion with a solution containing 500 nM free Ca2+ and external application of the BK channel opener phloretin (100 µM) shifted the activation threshold of BK channel currents toward more negative voltages of about −30 mV, which is close to the resting potential of the cells. The concentration of intracellular Ca2+ in fura-2-loaded 1321N1 cells was measured to be 235±19 nM and was increased to 472±25 nM after treatment with phloretin. Phloretin and another BK channel opener NS1619 (100 µM) reduced the migration velocity by about 50%. A similar reduction was observed following muscarinic stimulation of glioma cells with acetylcholine (100 µM). The effects of phloretin, NS1619 and acetylcholine on cell migration were completely abolished by co-application of the specific BK channel blockers paxilline (5 µM) and iberiotoxin (100 nM). The phloretin-induced increase in intracellular Ca2+ was unaffected by the removal of extracellular Ca2+ and co-application of paxilline. These findings indicate that glioma cell migration was inhibited through BK channel activation, independent of intracellular Ca2+.
         datePublished:2003-02-15T00:00:00Z
         dateModified:2003-02-15T00:00:00Z
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            Human Physiology
            Molecular Medicine
            Neurosciences
            Cell Biology
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      headline:BK channel openers inhibit migration of human glioma cells
      description:Large-conductance Ca2+-activated K+ channels (BK channels) are highly expressed in human glioma cells. However, less is known about their biological function in these cells. We used the patch-clamp technique to investigate activation properties of BK channels and time-lapse microscopy to evaluate the role of BK channel activation in migration of 1321N1 human glioma cells. In whole cells, internal perfusion with a solution containing 500 nM free Ca2+ and external application of the BK channel opener phloretin (100 µM) shifted the activation threshold of BK channel currents toward more negative voltages of about −30 mV, which is close to the resting potential of the cells. The concentration of intracellular Ca2+ in fura-2-loaded 1321N1 cells was measured to be 235±19 nM and was increased to 472±25 nM after treatment with phloretin. Phloretin and another BK channel opener NS1619 (100 µM) reduced the migration velocity by about 50%. A similar reduction was observed following muscarinic stimulation of glioma cells with acetylcholine (100 µM). The effects of phloretin, NS1619 and acetylcholine on cell migration were completely abolished by co-application of the specific BK channel blockers paxilline (5 µM) and iberiotoxin (100 nM). The phloretin-induced increase in intracellular Ca2+ was unaffected by the removal of extracellular Ca2+ and co-application of paxilline. These findings indicate that glioma cell migration was inhibited through BK channel activation, independent of intracellular Ca2+.
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         BK channel
         Glioma
         Migration
         Potassium channel opener
         Human Physiology
         Molecular Medicine
         Neurosciences
         Cell Biology
         Receptors
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